| Regulation of Histone Acetylation and Apoptosis by Trichostatin in HL-60 Cells |
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| 引用本文： | 李新刚,陈维凯,谷俊侠,崔国惠,陈燕. Regulation of Histone Acetylation and Apoptosis by Trichostatin in HL-60 Cells[J]. 华中科技大学学报(医学英德文版), 2004, 24(6): 572-574. DOI: 10.1007/BF02911358 |
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| 作者姓名： | 李新刚 陈维凯 谷俊侠 崔国惠 陈燕 |
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| 作者单位： | The Institute of Hematology，Union Hospital，Tongji Medical College，Huazhong University of Science and Technology，Wuhan 430022，China，The Institute of Hematology，Union Hospital，Tongji Medical College，Huazhong University of Science and Technology，Wuhan 430022，China，The Institute of Hematology，Union Hospital，Tongji Medical College，Huazhong University of Science and Technology，Wuhan 430022，China，The Institute of Hematology，Union Hospital，Tongji Medical College，Huazhong University of Science and Technology，Wuhan 430022，China，The Institute of Hematology，Union Hospital，Tongji Medical College，Huazhong University of Science and Technology，Wuhan 430022，China |
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| 摘 要： | TrichostatinA(TSA),akindoftypicalhistonedeacetylaseinhibitor(DAIS),wasisolatedfromthemetablitesofStreptomyceshygroscopicus.Recently,TSAwasfoundtoinducedifferentiationand/orapoptosisinsolidtumorsandleukemiccells.InvivoresultsshowedthatTSAcouldselectivelyin…
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| 关 键 词： | 细胞凋亡 单端孢霉烯A HL-60细胞 组蛋白 乙酰化作用 脱乙酰基酶抑制剂 抗癌作用 |
| 收稿时间： | 2004-02-01 |
Regulation of histone acetylation and apoptosis by trichostatin in HL-60 cells |
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| Li Xingang,Chen Weikai,Gu Junxia,Cui Guohui,Chen Yan. Regulation of histone acetylation and apoptosis by trichostatin in HL-60 cells[J]. Journal of Huazhong University of Science and Technology. Medical sciences, 2004, 24(6): 572-574. DOI: 10.1007/BF02911358 |
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| Authors: | Li Xingang Chen Weikai Gu Junxia Cui Guohui Chen Yan |
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| Affiliation: | The Institute of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China |
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| Abstract: | Summary: In order to examine the strong anticancer action and low toxicity of Trichostatin A (TSA), the effect of TSA was examined on the growth inhibition, acetylation of histone H_3 and apoptosis in HL-60 cells by employing MTT, immunocytochemical techniques, and Annexin-V-FITC/PI assay. Our results showed that TSA could inhibit proliferation of HL-60 cells in a time-and dose-dependent manner, and the IC_~50 at the 36th h was 100 ng/ml. The apoptosis-inducing effect of TSA on HL-60 cells was also time-and dose-dependent. But it didn't demonstrate apparent apoptosis induction in NPBMNCs within specific dose and time range. Both of the acetylation of histone H_3 in HL-60 cells and NPBMNCs increased significantly (P<0.05) after treated with 100 ng/ml TSA for 4 h. However, there was no significant differences between the two groups (P>0.05). It is concluded that TSA can inhibit growth and induce apoptosis of HL-60 cells in a time-and dose-dependent manner, and is able to selectively induce apoptosis in HL-60 cells but does not respond in NPBMNCs under the same conditions. The difference of TSA between HL-60 cells and NPBMNCs can't be explained by the regulation of histone acetylation. |
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| Keywords: | Trichostatin A deacetylase inhibitor histone acetylation apoptosis HL-60 cells |
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